Food Contaminants
Food contamination refers
to the presence in food of harmful chemicals and microorganisms which can cause
consumer illness where chemical food contamination is mostly attached with toxicity
or carcinogenic reactions while microbes are well known for fatal and nonfatal diseases.
The impact of chemical contaminants on
consumer health and well-being is often apparent only after many years of
processing prolonged exposure at low levels (e.g., cancer). Chemical
contaminants present in foods are often unaffected by thermal processing
(unlike most microbiological agents). Chemical contaminants can be classified
according to the source of contamination and the mechanism by which they enter
the food product. There are number of chemical food contaminants identified and
tested and regulated for the wellbeing of human race. These chemical come under
following categories:
Dioxins
Polychlorinated
biphenyls (PCBs)
Food allergens
Heavy metals
Melamine
Mycotoxins
Pesticides
Radiation
contamination
Veterinary drug
residues
Dioxins
Dioxins are a
class of chemical contaminants and it is also called as persistent organic
pollutants (POPs), meaning they take a long time to break down once they are in
the environment. Dioxin is a general name for a large group of chemical
compounds with similar structure. These compounds are made up of carbon,
oxygen, hydrogen and chlorine atoms. The number of the chlorine atoms and their
positions in the dioxin molecule are what determines the toxicity of different
dioxins. The most toxic dioxin has four chlorine atoms in positions 2, 3, 7 and
8. This dioxin ( 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin) is often referred to
as TCDD or “dioxin”. TCDD is the most studied and the most toxic of the
dioxins.
Dioxins are
formed during combustion processes such as waste incineration, forest fires,
and backyard trash burning, as well as during some industrial processes such as
paper pulp bleaching and herbicide manufacturing. Dioxins are highly toxic and
can cause cancer, reproductive and developmental problems, damage to the immune
system, and can interfere with hormones. The most toxic chemical in the class
is 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD). Dioxins are found throughout
the world in the environment and they accumulate in the food chain, mainly in
the fatty tissue of animals and more than 90% of human exposure is through
food, mainly meat and dairy products, fish and shellfish. The highest
environmental concentrations of dioxin are usually found in soil and sediment,
with much lower levels found in air and water.
Dioxins, Furans, PCBs
Dioxins, furans,
and polychlorinated biphenyls (PCBs) (All contain phenyl rings of carbon atoms)
are a class of similar chlorinated aromatic organic compounds, where Dioxins
have two phenyl rings connected by two oxygen atoms. On contrary, Furans have
one or two phenyl rings connected to a furan ring and PCBs have two phenyl
rings attached at one point. One or more chlorine atoms can attach to any
available carbon atom, allowing for 100 - 200 forms of each. Dioxins and
dioxin-like furans have no known commercial or natural use. They are produced
primarily during the incineration or burning of waste; the bleaching processes
used in pulp and paper mills; and the chemical syntheses of
trichlorophenoxyacetic acid, hexachlorophene, vinyl chloride, trichlorophenol,
and pentachlorophenol. PCBs were once synthesized for use as heat-exchanger,
transformer, and hydraulic fluids, and also used as additives to paints, oils,
window caulking, and floor tiles. Production of PCBs peaked in the early 1970s
and was banned in the United States after 1979.
Exposure
Human exposure to
PCDDs, PCDFs, and PCBs may occur through background (environmental) exposure,
and accidental and occupational contamination. Over 90 percent of human
background exposure is estimated to occur through the diet, with food from
animal origin being the predominant source. PCDD and PCDF contamination of food
is primarily caused by deposition of emissions from various sources (e.g. waste
incineration, production of chemicals) on farmland and water bodies followed by
bioaccumulation up terrestrial and aquatic food chains. Other sources may
include contaminated feed for cattle, chicken and farmed fish, improper
application of sewage sludge, flooding of pastures, waste effluents and certain
types of food processing. If the dioxin-like PCBs (non-ortho and mono-ortho
PCBs) are also considered, the daily TEQ intake can be a factor of 2-3 higher.
Special consumption habits, particularly one low in animal fat or consumption of
highly contaminated food stuffs may lead to lower or higher TEQ intake values,
respectively. Compared to adults, the daily intake of PCDDs/PCDFs and PCBs for
breast fed babies is still 1-2 orders of magnitude higher on a per body weight
basis. The latest WHO field study showed differences between the PCDD/PCDF and
PCB contamination of breast milk, with higher mean levels in industrialized
areas (10-35 pg I-TEQ/g milk fat) and lower mean levels in developing countries
(< 10 pg I-TEQ/g milk fat).
High
exposure may also be caused by food items accidentally contaminated. Known
examples are the contamination of edible oil, such as the Yusho (Japan) and
YuCheng (Taiwan) food poisoning. For a group of Yusho patients, average intake
by ingestion of the Kanemi rice oil contaminated with PCBs, PCDFs and
polychlorinated quarterphenyls (PCQs) was estimated at 154000 pg I-TEQ/kg
bw/day, which is five orders of magnitude higher than the reported average
background intake in several countries.
Mechanism of Action
A broad variety
of data primarily on TCDD but also on other members of the class of dioxin-like
compounds has shown the importance of the Ah (dioxin) receptor in mediating the
biological effects of dioxin where data have been collected in many
experimental models in multiple species including humans. The precise chain of
molecular events by which the ligand-activated receptor elicits these effects
is not yet fully understood. However, alterations in key biochemical and
cellular functions are expected to form the basis for dioxin toxicity.
Effects of Dioxins on Human Health
Short-term
exposure of humans to high levels of dioxins may result in skin lesions, such
as chloracne and patchy darkening of the skin, and altered liver function.
Long-term exposure is linked to impairment of the immune system, the developing
nervous system, the endocrine system and reproductive functions. Chronic
exposure of animals to dioxins has resulted in several types of cancer. The
developing fetus is most sensitive to dioxin exposure. Newborn, with rapidly
developing organ systems, may also be more vulnerable to certain effects. Some
people or groups of people may be exposed to higher levels of dioxins because
of their diet (e.g., high consumers of fish in certain parts of the world) or
their occupation (e.g., workers in the pulp and paper industry, in incineration
plants and at hazardous waste sites).
Prevention and Control of Dioxin Exposure
Proper
incineration of contaminated material is the best available method of
preventing and controlling exposure to dioxins. It can also destroy PCB-based
waste oils. The incineration process requires high temperatures, over 850°C.
For the destruction of large amounts of contaminated material, even higher
temperatures - 1000°C or more - are required. Trimming fat from meat and
consuming low fat dairy products may decrease the exposure to dioxin compounds.
Also, a balanced diet (including adequate amounts of fruits, vegetables and
cereals) will help to avoid excessive exposure from a single source. This is a
long-term strategy to reduce body burdens and is probably most relevant for
girls and young women to reduce exposure of the developing fetus and when
breastfeeding infants later on in life. However, the possibility for consumers
to reduce their own exposure is somewhat limited.
Reference:
http://www.who.int/mediacentre/factsheets/fs225/en/
http://www.who.int/ipcs/publications/en/exe-sum-final.pdf
http://unsolvedmysteries.oregonstate.edu/flow_02
http://www.greenfacts.org/en/dioxins/l-2/dioxins-1.htm